Adv Pharm Bull. 2022;12(2): 237-247.
doi: 10.34172/apb.2022.025
  Abstract View: 475
  PDF Download: 203

Review Article

Exendin-4 as a Versatile Therapeutic Agent for the Amelioration of Diabetic Changes

Hadi Rajabi 1 ORCID logo, Mahdi Ahmadi 2, Somayeh Aslani 3, Shirin Saberianpour 4, Reza Rahbarghazi 5,6* ORCID logo

1 Koc University Research Center for Translational Medicine (KUTTAM), Koc University School of Medicine, Istanbul, Turkey.
2 Tuberculosis and Lung Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
3 Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
4 Vascular and Endovascular Surgery Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
5 Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
6 Department of Applied Cell Sciences, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
*Corresponding Author: Reza Rahbarghazi, Tel: +9841 33363870, Email: rahbarghazir@tbzmed.ac.ir


Type 2 diabetes mellitus (T2DM) is a chronic metabolic abnormality leading to microvascular and macrovascular complications. Non-insulin Incretin mimic synthetic peptide exendin-4 was introduced as an anti-diabetic drug which helped diabetic patients with triggering insulin secretion; further researches have revealed an effective role of exendin-4 in treatment of T2DM related diseases. Exendin-4 is approximately similar to Glucagon-like peptide, thus it can bind to the glucagon-like peptide-1 receptor (GLP-1R) and activated different signaling pathways that are involved in various bioactivities such as apoptosis, insulin secretion and inactivation of microglial. In this review, we investigated the interesting role of exendin-4 in various kinds of T2DM related disorders through the activation of different signaling pathways.
Keywords: Diabetes complications, Exendin-4, Signaling pathways

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Submitted: 02 Jun 2020
Revision: 31 Oct 2020
Accepted: 29 Jan 2021
ePublished: 31 Jan 2021
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